Neutrophils predominate during the acute phase of the Paracoccidioides brasiliensis infection. Herein, we determined the role of the neutrophil during the early stages of experimental pulmonary paracoccidioidomycosis using a monoclonal antibody (mAb) specific for neutrophils. Male BALB/c mice were inoculated intranasally with 1.5 &times; 106 or 2 &times; 106 P. brasiliensis yeast cells. The mAb was administered 24&thinsp;h before infection, followed by doses every 48&thinsp;h until mice were sacrificed. Survival time was evaluated and mice were sacrificed at 48&thinsp;h and 96&thinsp;h after inoculation to assess cellularity, fungal load, cytokine/chemokine levels, and histopathological analysis. Neutrophils from mAb-treated mice were efficiently depleted (99.04%). Eighty percent of the mice treated with the mAb and infected with 1.5 &times; 106 yeast cells died during the first two weeks after infection. When mice were treated and infected with 2 &times; 106 yeast cells, 100% of them succumbed by the first week after infection. During the acute inflammatory response significant increases in numbers of eosinophils, fungal load and levels of proinflammatory cytokines/chemokines were observed in the mAb-treated mice. We also confirmed that neutrophils are an important source of IFN-&gamma; and IL-17. These results indicate that neutrophils are essential for protection as well as being important for regulating the early inflammatory immune response in experimental pulmonary paracoccidioidomycosis.

Mentions:
In other sets of experiments, we confirmed that neutrophils are a source of two important cytokines such as IFN-γ, which is necessary to activate macrophages and mount an effective antifungal response, and IL-17 considered one of the most important proinflammatory cytokines. Thus, near to 60% of the total leukocytes (CD45+)/IFN-γ producing cells corresponded to neutrophils (Figures 6(a)-6(b)). In the case of IL-17, neutrophils accounted for 73% of the total leukocytes (CD45+)/IL-17 producing cells (Figures 6(c)-6(d)).

Mentions:
In other sets of experiments, we confirmed that neutrophils are a source of two important cytokines such as IFN-γ, which is necessary to activate macrophages and mount an effective antifungal response, and IL-17 considered one of the most important proinflammatory cytokines. Thus, near to 60% of the total leukocytes (CD45+)/IFN-γ producing cells corresponded to neutrophils (Figures 6(a)-6(b)). In the case of IL-17, neutrophils accounted for 73% of the total leukocytes (CD45+)/IL-17 producing cells (Figures 6(c)-6(d)).

Neutrophils predominate during the acute phase of the Paracoccidioides brasiliensis infection. Herein, we determined the role of the neutrophil during the early stages of experimental pulmonary paracoccidioidomycosis using a monoclonal antibody (mAb) specific for neutrophils. Male BALB/c mice were inoculated intranasally with 1.5 &times; 106 or 2 &times; 106 P. brasiliensis yeast cells. The mAb was administered 24&thinsp;h before infection, followed by doses every 48&thinsp;h until mice were sacrificed. Survival time was evaluated and mice were sacrificed at 48&thinsp;h and 96&thinsp;h after inoculation to assess cellularity, fungal load, cytokine/chemokine levels, and histopathological analysis. Neutrophils from mAb-treated mice were efficiently depleted (99.04%). Eighty percent of the mice treated with the mAb and infected with 1.5 &times; 106 yeast cells died during the first two weeks after infection. When mice were treated and infected with 2 &times; 106 yeast cells, 100% of them succumbed by the first week after infection. During the acute inflammatory response significant increases in numbers of eosinophils, fungal load and levels of proinflammatory cytokines/chemokines were observed in the mAb-treated mice. We also confirmed that neutrophils are an important source of IFN-&gamma; and IL-17. These results indicate that neutrophils are essential for protection as well as being important for regulating the early inflammatory immune response in experimental pulmonary paracoccidioidomycosis.